Culprit Artery Localization in STEMI: Insights from a Cardiology Presentation

 
Localization of culprit artery in
Localization of culprit artery in
STEMI
STEMI
 
Topic presentation
Topic presentation
Speaker
Dr.Suneesh.K
Senior Resident, Dept. of Cardiology
Calicut Medical College
Introduction
Coronary circulation and blood supply of the heart
AWMI
IWMI
RVMI
PWMI
Conduction disturbances
Atrial Infarction
Exercises
 
 
 
Overview
Overview
 
15-09-2024
 
Introduction
Careful analysis of the surface ECG is highly useful in
localizing the culprit vessel and immediate prognostication
 
Helps in deciding the need for an aggressive reperfusion
strategy
 
ECG correlation of infarct related artery predict moratlity in
acute myocardial infarction
Prevalence of STEMI
Newby et al, GUSTO Study J Am Coll Cardiol1996;27:625-32
 
Coronary circulation
 
Left Main or left coronary artery
LAD
          Diagonal braches (D1, D2)
          Septal branches
Circumflex
          Marginal branches (M1, M2)
 
Right coronary  artery
Conus, sinoatrial branch
RV branch
Acute marginal branch
AV nodal branch
Posterior descending artery (PDA)
 
Blood supply of heart
LAD
Supplies the anterior, lateral, anterior two-thirds of septum, and
frequently the inferoapical segments of LV, including the
proximal part of bundle branches
 
RCA
Perfuses SA node (65%), AV node, postero-medial papillary
muscle, inferior part of LV, RV, and variably also the posterior
and lateral segments
Circumflex branch
Posterior wall and variably inferior and lateral segments
 
Posterior wall involvement 
 usually underestimated and
under treated
 
Blood supply of heart (contd..)
SA node – RCA in 65%
AV node – RCA in 90%
Bundle of His – Mainly RCA
RBB – LAD
LBB – L Ant branch – LAD
LBB - L Post branch – LAD & PDA
 
Blood supply of heart (contd..)
 
Dominance
Supplies circulation to the inferior wall and inferior
portion of the  posterior IVS
 
Dominant artery passes crux and IVS, giving rise to
posterolateral branches and PDA
 
Dominant artery also gives rise to the AV nodal branch
 
Nondominant artery is usually smaller in size and
terminates early in its respective AV groove
 
Dominance
RCA – 70%
LCX – 10%
Co- dominant – 20%
 
 
Right  dominant
 
 
Left  dominant
 
The concept of injury vector:
Direct and reciprocal changes
Injury vector is oriented towards the injured area and generates
STE in the leads facing the vector’s head
 
ST-segment depression in the leads facing the vector’s tail
(opposed leads)
 
Leads perpendicular to dominant vector will record an iso-
electrical ST segment
 
 
Proximal occlusion of long LAD
 
Distal occlusion of long LAD
 
 
 
Ischemia at a distance Vs reciprocal
changes
Patients with ST elevation in one territory often have ST depression in
other territories
 
The additional ST deviation may represent acute  ischemia due to coronary
artery disease in non infarct related arteries (ischemia at a distance)  or may
represent pure "mirror image" reciprocal changes
 
Most of the common patterns of remote ST depression probably represent
reciprocal changes and not “ischemia at a distance”
AWMI
AWMI
 
Anteroseptal zone: occlusion of the
LAD and its branches
Proximal to 1
st
 septal and 1
st
  diagonal branch (40%)
Distal to S and D (40%)
Proximal to D1 but distal to S1 (5-10%)
Proximal to S1 but distal to D1 (5-10%)
Selective D1–D2occlusion
Selective S1–S2 occlusion
 
Proximal LAD occlusion
(Dominance of Basal area)
 
 
Injury vector is directed anteriorly and upward, and somewhat to the right or  left
 
Proximal LAD occlusion
(Dominance of Basal area)
STE aVR and STE in V1 
>
 2.5 mm
ST depression in inferior leads and in V5
Abnormal Q in aVL
ST depression in the inferior wall (III +aVF ≥2.5
mm) is quite suggestive of a proximal occlusion of
LAD above D1
 
Proximal LAD occlusion
(Dominance of Basal area)
 
 
 
Distal LAD occlusion
(Dominance of inferoapical area)
 
Distal LAD occlusion
(Dominance of inferoapical area)
 
Inferior third of the LV & low-lateral involvement (apical
infarction)
 Injury vector is directed forward and left, and downward
STE in inferior leads (II > III) in addition to V3-V6
Slight ST-segment depression in aVR
Wide Q V4-V6 some times
Distal LAD occlusion
(Dominance of inferoapical area)
STE is seen in the precordial and inferior leads in the presence of
a STEMI due to the very proximal occlusion of the RCA
In this case the STE usually is V1>V3−4, while in a STEMI due
to the distal occlusion of the LAD the opposite occurs
(i.e., the STE is V1<V3−4)
 
 
 
 
 
1
st
 Diagonal not involved
(Dominance of septal area)-Proximal to S1
 
1
st
 Diagonal not involved
(Dominance of septal area)-Proximal to S1
 
 
Injury vector is directed anteriorly, to the right and sometimes downward
Antero-septal infarction
STE  in aVR and 
> 
2.5 mm STE in V1
ST elevation from V1to V3−4and II, III, and aVF
ST depression in V6, I and aVL
STE in V3R
RBBB/ QRBBB
 
1
st
 Diagonal not involved
(Dominance of septal area)-Proximal to S1
 
 
 
1
st
 Diagonal not involved
(Dominance of septal area)-Proximal to S1
 
First septal branch not included
(Dominance of Lateral area) – Prox to D1
 
 
Injury vector is directed anteriorly, upward, and somewhat to the left
ST  elevation lead AVL & lead I
Q left lateral leads
ST depression in Lead III > Lead II
ST depression in (III + aVF) ≥ 2.5 mm
 
First septal branch not included
(Dominance of Lateral area) – Prox to D1
 
First septal branch not included
(Dominance of Lateral area) – Prox to D1
 
First septal branch not included
(Dominance of Lateral area) – Prox to D1
 
ECG criteria to identify site of
occlusion in the LAD
 
 
 
New QRBBB in V1 is a specific but insensitive marker of proX LAD occlusion
New QRBBB in V1 is a specific but insensitive marker of proX LAD occlusion
Area affected -Mid-low anterior wall and part of the mid- and
often low-lateral wall
 
Injury vector is directed upward, to the left and forward
 
STE in I, aVL and 
precordial leads V2−V6 
(Variable)
 
ST depression in II, III, and VF (III >II)
 
Selective occlusion of the D1branch
 
Selective occlusion of the D1branch
 
Selective occlusion of the S1branch
Septal wall with occasionally certain extension toward
the anterior wall
Injury vector directed anteriorly, upward, and to the
right
STE in V1,V2, and aVR
ST depression in II, III, aVF (II>III), and V6
No ST elevation in aVL
 
Selective occlusion of the S1branch
Algorithm for ECG Identification of the Infarct-Related Artery in AW-STEMI
Engelen DJ, Gorgels AP, Cheriex EC et al 
J Am Coll Cardiol 1999; 34:389-95
IWMI
IWMI
 
Injury vector in RCA and LCX
 
 
Right coronary
 
Circumflex coronary
V5 and V6 are of little value in differentiating between RCA or Cx
occlusion. STE in these leads implies a larger area at risk
 
Occlusion of the RCA
ST elevation in III > II
ST depression in I and aVL -  aVL > I
ST depression in the right precordial leads is smaller than
STE in inferior leads
When occlusion is proximal to RV branches ST E in V1 >
V3 V4
 
 
When RCA is dominant, STE is seen in V5 and V6 (Local
injury vector)
Involvement of posterior wall
RCA very dominant or super dominant - STE elevation ≥ 2
mm in V5-V6 and ST depression in I and aVL
Eskola et al. 2004
 
 
Occlusion of the RCA (Contd..)
Occlusion of the LCX
ST- elevation in II ≥ III
ST elevation in I and aVL or isoelectric 
(rarely)
STE in II, III, and aVF is usually smaller than the ST
depression in right precordial leads
When LCX is quite dominant - ST depression in aVL, 
but
very rarely in I and STE 4-5 mm in v5-v6
ST depression in aVR - Involvement of either the LCX or the RCA with a large
posterolateral (PL) branch
The specificity and sensitivity for lead aVR to predict LCX involvement - 94%
and 70%, respectively
Zhang YZ et al . The value of ECG lead aVR
in the differential diagnosis of acute IWMI. Intern Med, 2007; 46: 795–799
Decrease in R-wave amplitude and an increase in S-wave amplitude with an
S/R ratio of  >1:3 in  aVL predict RCA occlusion, whereas an S/R ratio of 1:3
or less predict LCx occlusion
Assali AR et al. Electrocardiographic criteria for
predicting the culprit artery in IWMI. Am J Cardiol, 1999; 84: 87–89
 
 
 
Proximal occlusion of a very dominant LCX
First step:
Assess the ST-segment in lead I
STD
RCA
Isoelectric-
 Proceed to 2
nd
  step:
STE in II, III, aVF
STE
LCX
II > III
LCX
III > II
Proceed to 3
rd
 step:
 
Ʃ STD V1-V3
 
Ʃ STE II, III, aVF
> 1
 LCX
< 1
 RCA
 
Fiol M A et al;
Value of electrocardiographic algorithm based on “ups and
downs” of ST in assessment of a culprit artery in IWMI
Am J Cardiol, 2004; 94: 709–714
 
OM VS D1 occlusion
RVMI
RVMI
 
RV infarction
 
RV infarction
STE >1mm V3R and V4R
STE V1 > V2
High degree AV block
Sometimes STE in V1 with STD in V2 (Discordant
relationship)
STD in V3
 STE in III
Less than
0.5
0.5 to 1.2
More
than 1.2
LCx artery
Sens 84%
Spec 95%
Distal RCA
Sens 84%
Spec 93%
Proximal RCA
Sens 91%
Spec 91%
Kosuge M
, Kimura K, Ishikawa T et al.
New electrocardiographic criteria for predicting the culprit artery in
inferior wall acute myocardial infarction. Am J Cardiol, 1998; 82: 1318–1322
V4R in acute infero posterior MI
 
STE III>II
STD in I, aVL or both (>1mm)
RCA
Sensitivity 90%
Specificity 71%
PPV 94%
NPV 70%
STE I, aVL, V5 and V6
 
STD in V1,V2,V3
LCX
Sensitivity 83%
Specificity 96%
PPV 91%
NPV 93%
In addition, STE in V1, V4R, or both
Proximal RCA with RVMI
Sensitivity 79%
Specificity 100%
PPV 100%
NPV 88%
 
Zimetbaum et Al; NEJM 2003
STEMI due to proximal RCA occlusion
 
STEMI due to RCA occlusion distal to the RV
branches
 
 
Very dominant RCA occlusion distal to the
RV branches
Proximal occlusion of a very dominant LCX
 
Isolated RVMI
Minor changes in inferior leads, but STE prominent in leads
V1 and V2 and right precordial leads (V3R and V4R)
 
Due to either a small or collaterally filled RCA or an occlusion
of an RV branch only
 
 
PWMI
PWMI
 
Posterior wall involvement
ST depression in the precordial leads
May extend from V1 to V6 and indicate larger MI
Maximal ST depression in V4 – V6 is seen more in
three vessel disease and lower LVEF
Can occur both in RCA and Cx artery involvement
 
Posterior wall involvement
In case of LCX occlusion posteriorwall involvement is almost obligatory
 
Absence of precordial ST depression in inferior wall infarction is therefore strongly
suggestive of RCA involvement
 
Isolated ST depression V1-V3– LCx occlusion with a true PWMI or nonocclusive
myocardial ischemia
 
Max ST depression in V2 and V3 is predictive of LCx
 
V7 –V9 shows ST elevation even though less amplitude
True PWMI
ST depression in V1, R/S >1, and upright T wave
 
V1
 
V9
Marked down sloping ST depression in I, II, and V4 – V6 and
STE in aVR
aVR STE occurred more in LMCA than in LAD
V1 STE was less in LMCA than LAD
High mortality rate in those with higher STE in Avr
Yamaji H et al J Am Coll Cardiol 2001;38:1348-1354
 
Left main stem occlusion or
 triple vessel disease
 
Left main stem occlusion or
 triple vessel disease
Acute LMCA occlusion rare but causes serious
hemodynamic deterioration
 
More commonly, subtotal occlusion occurs with collaterals
filling from RCA 
 presents as Unstable angina
 
ECG of subtotal occlusion similar to triple vessel disease
 
 
Conduction disturbances
Conduction disturbances
 
AV conduction disturbances
AV nodal delay and block occurs with proximal RCA
involvement, frequently with RVMI
 
Higher in-hospital morbidity & mortality
 
Sub AV conduction disturbances
RBBB with or without hemiblock during acute AWMI
indicates proximal LAD
 
BBB or CHB indicates poor prognosis
 
LAHB in acute IWMI indicates additional LAD disease
 
Atrial infarction
Signs of atrial MI are seen in PTa segment
PTa segment elevation occurs in I, II, III, V5 or V6 or a
depression in precordial leads
Occurs in 10 % of inferoposterior MI
Isolated occurrence is rare
Proximal RCA or Cx
 
 
 
Acute MI : ECG subsets and correlated
infarct related artery and mortality
 
Gusto I cohort population Topol EJ; ed 1998
 
Limitations
Assessment of the site of occlusion of coronary vessel by ECG is most reliable in
case of 1
st
 MI
 
Impaired
Multivessel disease
Collateral circulation
When ventricular activation is prolonged as in
LVH
Preexistent LBBB
Preexcitation
Paced rhythm
 
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Dr. Suneesh K., a Senior Resident in the Dept. of Cardiology at Calicut Medical College, delves into the crucial role of ECG analysis in identifying the culprit artery during ST-elevation myocardial infarction (STEMI). This presentation covers coronary circulation, blood supply of the heart, prevalence of STEMI, and the significance of immediate prognosis based on ECG findings. Explore how surface ECG correlations can guide reperfusion strategies and predict mortality in acute myocardial infarction cases.

  • Cardiology
  • Culprit Artery
  • STEMI
  • ECG Analysis
  • Coronary Circulation

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  1. Localization of culprit artery in Localization of culprit artery in STEMI STEMI Topic presentation Speaker Dr.Suneesh.K Senior Resident, Dept. of Cardiology Calicut Medical College

  2. Overview Overview Introduction Coronary circulation and blood supply of the heart AWMI IWMI RVMI PWMI Conduction disturbances Atrial Infarction Exercises 15-09-2024

  3. Introduction Introduction Careful analysis of the surface ECG is highly useful in localizing the culprit vessel and immediate prognostication Helps in deciding the need for an aggressive reperfusion strategy ECG correlation of infarct related artery predict moratlity in acute myocardial infarction

  4. Prevalence of STEMI Prevalence of STEMI Inferior 58% Anterior 39% Other 3% Newby et al, GUSTO Study J Am Coll Cardiol1996;27:625-32

  5. Coronary circulation Coronary circulation Left Main or left coronary artery LAD Diagonal braches (D1, D2) Septal branches Circumflex Marginal branches (M1, M2) Right coronary artery Conus, sinoatrial branch RV branch Acute marginal branch AV nodal branch Posterior descending artery (PDA)

  6. Blood supply of heart Blood supply of heart LAD Supplies the anterior, lateral, anterior two-thirds of septum, and frequently the inferoapical segments of LV, including the proximal part of bundle branches RCA Perfuses SA node (65%), AV node, postero-medial papillary muscle, inferior part of LV, RV, and variably also the posterior and lateral segments

  7. Blood supply of heart (contd..) Blood supply of heart (contd..) Circumflex branch Posterior wall and variably inferior and lateral segments Posterior wall involvement usually underestimated and under treated

  8. Blood supply of heart (contd..) Blood supply of heart (contd..) SA node RCA in 65% AV node RCA in 90% Bundle of His Mainly RCA RBB LAD LBB L Ant branch LAD LBB - L Post branch LAD & PDA

  9. Dominance Dominance Supplies circulation to the inferior wall and inferior portion of the posterior IVS Dominant artery passes crux and IVS, giving rise to posterolateral branches and PDA Dominant artery also gives rise to the AV nodal branch Nondominant artery is usually smaller in size and terminates early in its respective AV groove

  10. Dominance Dominance RCA 70% LCX 10% Co- dominant 20%

  11. Right dominant Right dominant

  12. Left dominant Left dominant

  13. The concept of injury vector: The concept of injury vector: Direct and reciprocal changes Direct and reciprocal changes Injury vector is oriented towards the injured area and generates STE in the leads facing the vector s head ST-segment depression in the leads facing the vector s tail (opposed leads) Leads perpendicular to dominant vector will record an iso- electrical ST segment

  14. Proximal occlusion of long LAD Proximal occlusion of long LAD Distal occlusion of long LAD Distal occlusion of long LAD

  15. Ischemia at a distance Vs reciprocal Ischemia at a distance Vs reciprocal changes changes Patients with ST elevation in one territory often have ST depression in other territories The additional ST deviation may represent acute ischemia due to coronary artery disease in non infarct related arteries (ischemia at a distance) or may represent pure "mirror image" reciprocal changes Most of the common patterns of remote ST depression probably represent reciprocal changes and not ischemia at a distance

  16. AWMI AWMI

  17. Anteroseptal zone: occlusion of the Anteroseptal zone: occlusion of the LAD and its branches LAD and its branches Proximal to 1st septal and 1st diagonal branch (40%) Distal to S and D (40%) Proximal to D1 but distal to S1 (5-10%) Proximal to S1 but distal to D1 (5-10%) Selective D1 D2occlusion Selective S1 S2 occlusion

  18. Proximal LAD occlusion (Dominance of Basal area) Injury vector is directed anteriorly and upward, and somewhat to the right or left

  19. Proximal LAD occlusion (Dominance of Basal area)

  20. Proximal LAD occlusion (Dominance of Basal area) STE aVR and STE in V1 > 2.5 mm ST depression in inferior leads and in V5 Abnormal Q in aVL ST depression in the inferior wall (III +aVF 2.5 mm) is quite suggestive of a proximal occlusion of LAD above D1

  21. Distal LAD occlusion Distal LAD occlusion (Dominance of inferoapical area) (Dominance of inferoapical area)

  22. Distal LAD occlusion Distal LAD occlusion (Dominance of inferoapical area) (Dominance of inferoapical area)

  23. Distal LAD occlusion Distal LAD occlusion (Dominance of inferoapical area) (Dominance of inferoapical area) Inferior third of the LV & low-lateral involvement (apical infarction) STE is seen in the precordial and inferior leads in the presence of Injury vector is directed forward and left, and downward a STEMI due to the very proximal occlusion of the RCA STE in inferior leads (II > III) in addition to V3-V6 In this case the STE usually is V1>V3 4, while in a STEMI due Slight ST-segment depression in aVR to the distal occlusion of the LAD the opposite occurs Wide Q V4-V6 some times (i.e., the STE is V1<V3 4)

  24. 1 1st st Diagonal not involved Diagonal not involved (Dominance of septal area) (Dominance of septal area)- -Proximal to S1 Proximal to S1

  25. 1 1st st Diagonal not involved Diagonal not involved (Dominance of septal area) (Dominance of septal area)- -Proximal to S1 Proximal to S1 Injury vector is directed anteriorly, to the right and sometimes downward

  26. 1 1st st Diagonal not involved Diagonal not involved (Dominance of septal area) (Dominance of septal area)- -Proximal to S1 Proximal to S1 Antero-septal infarction STE in aVR and > 2.5 mm STE in V1 ST elevation from V1to V3 4and II, III, and aVF ST depression in V6, I and aVL STE in V3R RBBB/ QRBBB

  27. 1 1st st Diagonal not involved Diagonal not involved (Dominance of septal area) (Dominance of septal area)- -Proximal to S1 Proximal to S1

  28. First septal branch not included First septal branch not included (Dominance of Lateral area) (Dominance of Lateral area) Prox to D1 Prox to D1 Injury vector is directed anteriorly, upward, and somewhat to the left

  29. First septal branch not included First septal branch not included (Dominance of Lateral area) (Dominance of Lateral area) Prox to D1 Prox to D1 ST elevation lead AVL & lead I Q left lateral leads ST depression in Lead III > Lead II ST depression in (III + aVF) 2.5 mm

  30. First septal branch not included First septal branch not included (Dominance of Lateral area) (Dominance of Lateral area) Prox to D1 Prox to D1

  31. First septal branch not included First septal branch not included (Dominance of Lateral area) (Dominance of Lateral area) Prox to D1 Prox to D1

  32. ECG criteria to identify site of ECG criteria to identify site of occlusion in the LAD occlusion in the LAD

  33. New QRBBB in V1 is a specific but insensitive marker of proX LAD occlusion

  34. Selective occlusion of the D1branch Selective occlusion of the D1branch Area affected -Mid-low anterior wall and part of the mid- and often low-lateral wall Injury vector is directed upward, to the left and forward STE in I, aVL and precordial leads V2 V6 (Variable) ST depression in II, III, and VF (III >II)

  35. Selective occlusion of the D1branch Selective occlusion of the D1branch

  36. Selective occlusion of the S1branch Selective occlusion of the S1branch Septal wall with occasionally certain extension toward the anterior wall Injury vector directed anteriorly, upward, and to the right STE in V1,V2, and aVR ST depression in II, III, aVF (II>III), and V6 No ST elevation in aVL

  37. Selective occlusion of the S1branch Selective occlusion of the S1branch

  38. Algorithm for ECG Identification of the Infarct-Related Artery in AW-STEMI Engelen DJ, Gorgels AP, Cheriex EC et al J Am Coll Cardiol 1999; 34:389-95

  39. IWMI IWMI

  40. Injury vector in RCA and LCX Injury vector in RCA and LCX

  41. Right coronary Right coronary Circumflex coronary Circumflex coronary Inferoseptal ischemia Inferoposterolateral ischemia Vector directed to III Directed to II STE III > II STE II > III ST depression in aVL>I STE I or aVL or both RV can be involved True PWMI can occur V5 and V6 are of little value in differentiating between RCA or Cx occlusion. STE in these leads implies a larger area at risk

  42. Occlusion of the RCA Occlusion of the RCA ST elevation in III > II ST depression in I and aVL - aVL > I ST depression in the right precordial leads is smaller than STE in inferior leads When occlusion is proximal to RV branches ST E in V1 > V3 V4

  43. Occlusion of the RCA (Contd..) Occlusion of the RCA (Contd..) When RCA is dominant, STE is seen in V5 and V6 (Local injury vector) Involvement of posterior wall RCA very dominant or super dominant - STE elevation 2 mm in V5-V6 and ST depression in I and aVL Eskola et al. 2004

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